BUFFALO, N.Y. -- Iron is the workhorse of trace minerals. An essential component of red blood cells, disruption of iron levels in the body will result in a myriad of serious conditions, and life cannot be sustained without it.
In novel research, investigators at the University at Buffalos School of Public Health and Health Professions, have learned that iron is only one half of an all-important duo of trace minerals -- the other being copper -- that work in tandem to maintain proper iron balance, or homeostasis.
It appears the workhorse has a helper.
James F. Collins, Ph.D., UB assistant professor of exercise and nutrition sciences and biochemistry, discovered that when iron-absorption by cells lining the small intestine decreases during iron-deficient states, copper absorption increases.
Collins now is exploring the relationship between these two trace minerals through a $1.38 million grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).
The work will be carried out using established models of intestinal iron absorption in humans, including iron and iron/copper-deficient rodents and cultured intestinal epithelial cells.
This project is intended to test the overall hypothesis that increased copper transport during iron-deficiency is critical to enhance certain aspects of intestinal iron absorption, said Collins.
Iron or copper deficiency causes anemia, and abnormal intestinal iron transport is associated with several common human pathologies, including anemia of chronic disease (ACD) and hereditary hemochromatosis (HH), different forms of which result from several common genetic defects.
HH is an inherited metabolic disorder characterized by abnormally high absorption of dietary iron, which is deposited in body tissues and organs, where it may become toxic. ACD is a blood disorder caused by low body iron levels resulting from any medical condition that affects the production and lifespan of red bloo'"/>

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